Michael Curtis Petriello (hb4747)

 313-577-1089

Specifically, I am interested in how chemical and non-chemical stressors such as diet can interact to increase the risk of inflammatory diseases. This paradigm is exemplified by my currently funded K99/R00 entitled “TMAO is a biomarker of dioxin-like pollutant exposure and cardiometabolic disease”. Trimethylamine N-oxide (TMAO) is a novel biomarker of cardiometabolic disease and we are interested in how exposures to certain classes of pollutants may increase circulating levels of this diet-derived metabolite. We have shown that dioxin-like pollutants may increase TMAO levels by increasing the hepatic expression of enzymes directly related to TMAO formation (FMO3), and/or by modulating gut microbiota.

Current Funding:

Role: Principal Investigator
Co-Is: Samuel Zilioli
Title: “PFAS and Cardiovascular Risk among African American Adults: A Prospective
Investigation of Putative Biological Mechanisms.”
The goal of this grant is to determine if PFAS associate with CVD risk factors in Detroit residents
Source: ACHIEVE GreatER Pilot

Role: Principal Investigator, R00ES028734-01A1
Title: “TMAO is a biomarker of dioxin-like pollutant exposure and cardiometabolic disease.”
The primary objective is to determine if the microbiota-derived metabolite TMAO is a
mechanism linking exposures to dioxin-like pollutants and cardiometabolic disease risk.
Source: NIH/NIEHS

Role: Principal Investigator
Co-Is: Phil Levy
Title: “Impact of PFAS pollutant exposures on cardiovascular disease markers in African
American residents of Detroit and interventions with Statins.”
The goal of this grant is to determine if lipid lowering therapy reduces the toxicity of PFAS in mice and
humans.
Source: DMC Foundation

Role: Principal Investigator
ECHO OIF
Co-Is: Douglas Ruden (WSU), Andrea Cassidy-Bushrow (HFHS), Kimberly McKee, Jackie Goodrich
(UofM).
Title: “Impacts of environmental chemical exposures on gut microbiota and microbiota-derived
metabolites in mothers and children.” The major goal of this study is to determine if PFAS
exposures during pregnancy modulate maternal gut microbiota and the trajectory of microbiota
development in the offspring.
Source: NIH

Role: Subcontract PI
Co-Is: Jackie Goodrich (UofM) and Courtney Carignan (MSU)
Title: “Exposure to perfluoroalkyl substances (PFAS) and maternal antibody response.” The
major goal of this study is to determine if PFAS exposures during pregnancy modulate antibody
response to Covid-19 vaccination.
Source: NIH

Role: Principal Investigator
Co-Is: Lauren Petrick (Mt. Sinai) and Jackie Goodrich (UofM)
Title: “Impact of PFAS exposures on endogenous metabolites in Michigan mothers.”
The primary objective of this Pilot and Feasibility study from the Human Health Exposure
Analysis Resource (HHEAR) is to measure PFAS and metabolites from maternal serum from
100 Michigan mothers in a single LC-MS/MS run.
Source: NIH/HHEAR

 Roy B*, Yang Z*, Pan G, Roth K, Agarwal M, Sharma R, Petriello MC#, Palaniyandi SS#
(shared corresponding authorship). Exposure to the Dioxin-like Pollutant PCB 126 Afflicts Coronary Endothelial Cells via Increasing 4-Hydroxy-2 Nonenal: A Role for Aldehyde
Dehydrogenase 2. Toxics. 2022; 10(6):328. https://doi.org/10.3390/toxics10060328.

Petriello MC, Mottaleb MA, Serio TC, Balyan B, Cave MC, Pavuk M, Birnbaum LS, Morris AJ. Serum concentrations of legacy and emerging per- and polyfluoroalkyl substances in the Anniston Community Health Surveys (ACHS I and ACHS II). Environ Int. 2022 Jan;158:106907. doi: 10.1016/j.envint.2021.106907. Epub 2021 Nov 8. PMID: 34763231.

Roth K, Yang Z, Agarwal M, Liu W, Peng Z, Long Z, Birbeck J, Westrick J, Liu W, Petriello MC. Exposure to a mixture of legacy, alternative, and replacement per- and polyfluoroalkyl substances (PFAS) results in sex-dependent modulation of cholesterol metabolism and liver injury. Environ Int. 2021 Dec;157:106843. doi: 10.1016/j.envint.2021.106843. Epub 2021 Aug
31. PMID: 34479135

Petriello MC, Hoffman JB, Vsevolozhskaya O, Morris AJ, Hennig B: Dioxin-like PCB 126 increases intestinal inflammation and disrupts gut microbiota and metabolic homeostasis. Environmental Pollution. 2018 Nov;242(Part A):1022-1032. doi: 10.1016/j.envpol.2018.07.039. Epub 2018 Jul 17. PMID: 30373033

Petriello MC, Charnigo R, Sunkara M, Soman S, Pavuk M, Birnbaum L, Morris AJ, Hennig B.: Relationship between serum trimethylamine N-oxide and exposure to dioxin-like pollutants. Environmental Research. 2018 Apr;162:211-218. doi: 10.1016/j.envres.2018.01.007. Epub 2018 Jan 30. PMID: 29353125.

Petriello MC, Brandon JA, Hoffman J, Wang C, Tripathi H, Abdel-Latif A, Ye X, Li X, Yang L, Lee E, Soman S, Barney J, Wahlang B, Hennig B, Morris AJ,: Dioxin-like PCB 126 increases systemic inflammation and accelerates atherosclerosis in lean LDL receptor deficient mice. Toxicological Sciences. 2018 Apr 1;162(2):548-558. doi: 10.1093/toxsci/kfx275. PMID: 29216392.

Petriello MC, Hoffman J, Sunkara, Wahlang B, Perkins JT, Morris AJ, Hennig B: Dioxin-like pollutants increase hepatic flavin containing monooxygenase (FMO3) expression to promote synthesis of the pro-atherogenic nutrient biomarker Trimethylamine N-oxide from dietary precursors. Journal of Nutritional Biochemistry. 2016 Jul;33:145-53. doi: 10.1016/j.jnutbio.2016.03.016. Epub 2016 Apr 1. PMID: 27155921

AlSiraj Y, Chen X, Thatcher SE, Temel RE, Cai L, Blalock E, Katz W, Ali HM, Petriello M, Deng P, Morris AJ, Wang X, Lusis AJ, Arnold AP, Reue K, Thompson K, Tso P, Cassis LA. XX sex chromosome complement promotes atherosclerosis in mice. Nature Communications. 2019 June 14; 10(1):2631. doi: 10.1038/s41467-019-10462-z. PMID: 31201301

6135 Woodward Avenue
IBio Room 2128
Detroit, MI 48202

313-577-1089

** Please visit my lab webpage for more information ** www.petriellolab.org

The goals of my research are directly relatable to understanding mechanisms that link nutrition and toxicology and may lead to translatable prevention strategies that may limit pollutant-induced metabolic disorders such as diabetes, obesity, and cardiovascular disease especially in at-risk populations. I also have strong experience and interest in using large data sets to uncover novel associations of environmental risk and cardiovascular disease as well as working with underserved communities that face multiple chemical and non-chemical stressors.

Overall, I aim to investigate biomarkers that link environmental exposures, diet, and metabolic diseases in human populations and to test mechanisms of toxicity using mouse models of cardiometabolic disease.

Harvard Medical (Boston Children’s Hospital), Boston, MA,Visiting Scientist, Endocrinology, 2016

Muhlenberg College, Allentown, PA, BS, Biology / Environmental Science, 05/2010
University of Kentucky, Lexington, KY, Ph.D., Toxicology, 05/2015

• Toxicology
• Environmental Health
• Cardiovascular Medicine
• Metabolomics/Mass Spectrometry
• Nutritional Sciences

University of Kentucky, Lexington, KY, Postdoctoral Fellow, Cardiovascular Research Institute, 2016-2019

Current:

TMAO is a biomarker of dioxin-like pollutant exposure and cardiometabolic disease– K99R00ES028734

The goal of this career development grant is to increase knowledge in analytical chemistry, biostatistics and epidemiology with a focus on mechanisms linking diet and dioxin-like pollutant exposure to increased risk of atherosclerosis and cardiometabolic disease.

Past:

Transcriptional Effects of Per and Poly Fluorinated Alkyl Substances

The goal of this internal NIEHS Environmental Health Sciences Core Center grant is to provide funding to optimize high throughput screens to identify transcription factors relevant to PFAS toxicity.

NIH T32 Training Grant Recipient – 5T32HL091812-08

Post doctoral Fellowship in cardiovascular research. “Clinical Scholars in Cardiovascular Science”.

American Heart Association Great Rivers Affiliate Predoctoral Fellowship

Project title: Novel methodologies to study anti-inflammatory nitro-fatty acids.

Petriellolab.org

Lexington, KY VA medical Center - WOC appointment

Selected publications:

Petriello MC, Hoffman JB, Vsevolozhskaya O, Morris AJ, Hennig B: Dioxin-like PCB 126 increases intestinal inflammation and disrupts gut microbiota and metabolic homeostasis. Environmental Pollution. 2018 Nov;242(Part A):1022-1032. doi: 10.1016/j.envpol.2018.07.039. Epub 2018 Jul 17. PMID: 30373033

Petriello MC, Charnigo R, Sunkara M, Soman S, Pavuk M, Birnbaum L, Morris AJ, Hennig B.: Relationship between serum trimethylamine N-oxide and exposure to dioxin-like pollutants. Environmental Research. 2018 Apr;162:211-218. doi: 10.1016/j.envres.2018.01.007. Epub 2018 Jan 30. PMID: 29353125.

Petriello MC, Brandon JA, Hoffman J, Wang C, Tripathi H, Abdel-Latif A, Ye X, Li X, Yang L, Lee E, Soman S, Barney J, Wahlang B, Hennig B, Morris AJ,: Dioxin-like PCB 126 increases systemic inflammation and accelerates atherosclerosis in lean LDL receptor deficient mice. Toxicological Sciences. 2018 Apr 1;162(2):548-558. doi: 10.1093/toxsci/kfx275. PMID: 29216392.

Petriello MC, Hoffman J, Sunkara, Wahlang B, Perkins JT, Morris AJ, Hennig B: Dioxin-like pollutants increase hepatic flavin containing monooxygenase (FMO3) expression to promote synthesis of the pro-atherogenic nutrient biomarker Trimethylamine N-oxide from dietary precursors. Journal of Nutritional Biochemistry. 2016 Jul;33:145-53. doi: 10.1016/j.jnutbio.2016.03.016. Epub 2016 Apr 1. PMID: 27155921

AlSiraj Y, Chen X, Thatcher SE, Temel RE, Cai L, Blalock E, Katz W, Ali HM, Petriello M, Deng P, Morris AJ, Wang X, Lusis AJ, Arnold AP, Reue K, Thompson K, Tso P, Cassis LA. XX sex chromosome complement promotes atherosclerosis in mice. Nature Communications. 2019 June 14; 10(1):2631. doi: 10.1038/s41467-019-10462-z. PMID: 31201301